Chest
Inflammation of the Airways and Lung Parenchyma in COPD: Role of T Cells
Section snippets
The Cellular Inflammatory Infiltrate in the Airways
The earliest, and constant pathological abnormality in the airway of smokers is the cellular inflammatory infiltrate throughout the wall. Inflammation per se may be responsible for mild airflow limitation.7,8,9 Indeed, it has been suggested that inflammation may lead to functional bronchiolar constriction by releasing mediators that may act directly on bronchiolar smooth muscle.10 The chronicity of inflammation would, in turn, produce other changes such as airways fibrosis, and may increase the
Biochemical Markers of Early Lung Inflammation in Smokers
Despite its nonspecific nature, the early inflammatory response to cigarette smoke is probably crucial to the development of subsequent tissue damage and disease in susceptible individuals. Neutrophils and macrophages can potentially produce large quantities of proteases, of which the various elastase enzymes have attracted the most attention as likely causes of loss of elastic recoil and the destruction of the elastic fibers in the lung parenchyma. Indeed, lung specimens from patients with
Differences in Airway Inflammation Between Smokers With and Without COPD
It is reasonable to hypothesize that the inflammatory process in the airways of smokers destined to develop COPD differs from that in individuals who are resistant to the effects of cigarette smoke. This has proved to be difficult to demonstrate, and it remains unclear whether quantitative or qualitative differences in the inflammatory response account for the development of COPD in susceptible subjects. A logical cell to consider first was the neutrophil, which is characteristically present in
Potential Role of the T cells in COPD
The findings of increased numbers of T lymphocytes and especially CD8+ T cells only in lung specimens of smokers who develop COPD is intriguing and supports the notion that tissue injury is dependent on T-cell activity. If so, progress in understanding the transition from lung inflammation to COPD in smokers will depend on an improved understanding of the factors that favor the proliferation of T cells in the lungs, which is an immunologic response.
Based on the known physiologic behavior of T
CD8+ T-Cell Inflammation in Emphysematous Lungs
One of the important consequences of the effector functions of cytotoxic CD8+ T cells is the apoptosis of target cells, and it would not be surprising that apoptosis plays a role in the destruction of lung tissue in patients with emphysema. Majo et al47 have reported that, in smokers with emphysema, both the degree of apoptosis and the number of CD8+ T cells in the alveolar wall increased in parallel with the amount of smoke inhaled (Fig 3). This suggests that the proliferation of cytotoxic T
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